Performance and stall limits of a YTF30-P-1 turbofan engine with uniform inlet flow

Performance and stall limits of YTF30-P-1 turbofan engine with uniform compressor inlet flo

Engineering of next generation cyber-physical automation system architectures

Cyber-Physical-Systems (CPS) enable flexible and reconfigurable realization of automation system architectures, utilizing distributed control architectures with non-hierarchical modules linked together through different communication systems. Several control system architectures have been developed and validated in the past years by research groups. However, there is still a lack of implementation in industry. The intention of this work is to provide a summary of current alternative control system architectures that could be applied in industrial automation domain as well as a review of their commonalities. The aim is to point out the differences between the traditional centralized and hierarchical architectures to discussed ones, which rely on decentralized decision-making and control. Challenges and impacts that industries and engineers face in the process of adopting decentralized control architectures are discussed, analysing the obstacles for industrial acceptance and the new necessary interdisciplinary engineering skills. Finally, an outlook of possible mitigation and migration actions required to implement the decentralized control architectures is addressed.The authors would like to thank the European Commission for the support, and the partners of the EU Horizon 2020 project PERFoRM (2016b) for the fruitful discussions. The PERFoRM project has received funding from the European Union’s Horizon 2020 research and innovation programme under grant agreement No 680435.info:eu-repo/semantics/publishedVersio

Enzymfreisetzung und Aktivierung der Kallikrein-Kinin-Systeme bei experimenteller Pankreatitis

Das klinische Bild der akuten Pankreatitis wird entscheidend durch die sekundäre Schädigung von Herz-Kreislauf-System, Lunge und Niere bestimmt. Ziel der vorliegenden Untersuchung war es, durch Messungen in venösem Pankreasblut, Pankreaslymphe und Peritonealexsudat die Kompartimente zu bestimmen, über die die systemischen Schädigungen vermittelt werden. An anästhesierten Schweinen wurden die systemischen, hämodynamischen Parameter durch gesteuerte Volumentherapie konstant gehalten. Die Schweine wurden randomisiert der Kontrollgruppe (n = 9) oder einer der Pankreatitisgruppen zugeteilt (jeweils n = 10). Die Pankreatitis wurde durch Infusion von freier Fettsäure in die Pankreasarterien (FFS) oder durch Infusion einer 5%igen Natrium-Taurocholat-Lösung retrograd in den Pankreasgang (NaT) ausgelöst. Nach Isolation des Pankreas wurde venöses Pankreasblut, Pankreaslymphe und Peritonealexsudat gewonnen und die Aktivität von Lipase, Phospholipase A und Plasmaprokallikrein sowie die Konzentration von Organkallikrein und Kininogen bestimmt. In beiden Pankreatitismodellen fand sich ein Anstieg der Enzymaktivitäten. Die höchsten Aktivitäten fanden sich im Peritonealexsudat (Phospholipase A nach 40 min: Kontrolle 10,0 U/1, NaT 72,2 U/1). In beiden Pankreatitismodellen fanden sich außerdem Hinweise für eine Aktivierung des Organkallikrein-Kinin-Systems durch den Anstieg der Organkallikreinkonzentration und den Abfall der Gesamtkininogenkonzentration. Die stärksten Veränderungen fanden sich wieder im Peritonealexsudat (Organkallikrein nach 40 min: Kontrolle 14,7 ng/ml, NaT 452 ng/ml).The clinical course of acute pancreatitis is strongly influenced by secondary cardiac, pulmonary and renal damage. The aim of the present study was to gather information about the compartment promoting the systemic damage. Therefore the activity of lipase, phospholipase A and plasmaprokallikrein and the concentration of tissue kallikrein and kininogen were measured in portal venous blood, pancreatic lymph and peritoneal exudate. Anaesthetized pigs were subjected to fluid resuscitation to keep systemic haemodynamic parameters constant. The pancreas was isolated in situ. The pigs were randomly assigned to a control group (n = 9) or one of the two pancreatitis groups (n = 10 each). Pancreatitis was induced by i.a. infusion of free fatty acid (FFS) or retrograde infusion of 5 % sodium taurocholate intraductally (NaT). In both pancreatitis groups the activity of lipase and phospholipase A increased. The most pronounced changes were seen in the peritoneal exsudate (phospholipase A activity 40 min after induction: control 10.0 U/1, NaT 72.2 U/1). In both pancreatitis groups there was evidence for activation of the tissue kallikreinkinin system in the form of an increase in the kallikrein concentration and a decrease in the kininogen concentration. Again the changes were most pronounced in the peritoneal exsudate (tissue kallikrein 40 min after induction: control 14.7 ng/ml, NaT 452 ng/ml)

Angiogenesis in tissue engineering : Breathing life into constructed tissue substitutes

Long-term function of three-dimensional (3D) tissue constructs depends on adequate vascularization after implantation. Accordingly, research in tissue engineering has focused on the analysis of angiogenesis. For this purpose, 2 sophisticated in vivo models (the chorioallantoic membrane and the dorsal skinfold chamber) have recently been introduced in tissue engineering research, allowing a more detailed analysis of angiogenic dysfunction and engraftment failure. To achieve vascularization of tissue constructs, several approaches are currently under investigation. These include the modification of biomaterial properties of scaffolds and the stimulation of blood vessel development and maturation by different growth factors using slow-release devices through pre-encapsulated microspheres. Moreover, new microvascular networks in tissue substitutes can be engineered by using endothelial cells and stem cells or by creating arteriovenous shunt loops. Nonetheless, the currently used techniques are not sufficient to induce the rapid vascularization necessary for an adequate cellular oxygen supply. Thus, future directions of research should focus on the creation of microvascular networks within 3D tissue constructs in vitro before implantation or by co-stimulation of angiogenesis and parenchymal cell proliferation to engineer the vascularized tissue substitute in situ

Microcirculatory alterations in ischemia–reperfusion injury and sepsis: effects of activated protein C and thrombin inhibition

Experimental studies in ischemia–reperfusion and sepsis indicate that activated protein C (APC) has direct anti-inflammatory effects at a cellular level. In vivo, however, the mechanisms of action have not been characterized thus far. Intravital multifluorescence microscopy represents an elegant way of studying the effect of APC on endotoxin-induced leukocyte–endothelial-cell interaction and nutritive capillary perfusion failure. These studies have clarified that APC effectively reduces leukocyte rolling and leukocyte firm adhesion in systemic endotoxemia. Protection from leukocytic inflammation is probably mediated by a modulation of adhesion molecule expression on the surface of leukocytes and endothelial cells. Of interest, the action of APC and antithrombin in endotoxin-induced leukocyte–endothelial-cell interaction differs in that APC inhibits both rolling and subsequent firm adhesion, whereas antithrombin exclusively reduces the firm adhesion step. The biological significance of this differential regulation of inflammation remains unclear, since both proteins are capable of reducing sepsis-induced capillary perfusion failure. To elucidate whether the action of APC and antithrombin is mediated by inhibition of thrombin, the specific thrombin inhibitor hirudin has been examined in a sepsis microcirculation model. Strikingly, hirudin was not capable of protecting from sepsis-induced microcirculatory dysfunction, but induced a further increase of leukocyte–endothelial-cell interactions and aggravated capillary perfusion failure when compared with nontreated controls. Thus, the action of APC on the microcirculatory level in systemic endotoxemia is unlikely to be caused by a thrombin inhibition-associated anticoagulatory action

Forest Cover Changes in Tropical South and Central America from 1990 to 2005 and Related Carbon Emissions and Removals.

This paper outlines the methods and results for monitoring forest change and resulting carbon emissions for the 1990-2000 and 200-2005 periods carried out over tropical Central and South America. To produce our forest change estimates we used a systematic sample of medium resolution satellite data processed to forest change maps covering 1230 sites of 20 km by 20 km, each located at the degree confluence. Biomass data were spatially associated to each individual sample site so that annual carbon emissions could be estimated. For our study area we estimate that forest cover in the study area had fallen from 763 Mha (s.e. 10 Mha) in 1990 to 715 Mha (s.e. 10 Mha) in 2005. During the same period other wooded land (i.e., non-forest woody vegetation) had fallen from 191 Mha (s.e. 5.5 Mha) to 184 Mha (s.e. 5.5 Mha). This equates to an annual gross loss of 3.74 Mha·y−1 of forests (0.50% annually) between 1990 and 2000, rising to 4.40 Mha·y−1 in the early 2000s (0.61% annually), with Brazil accounting for 69% of the total losses. The annual carbon emissions from the combined loss of forests and other wooded land were calculated to be 482 MtC·y−1 (s.e. 29 MtC·y−1) for the 1990s, and 583 MtC·y−1 (s.e. 48 MtC·y−1) for the 2000 to 2005 period. Our maximum estimate of sinks from forest regrowth in tropical South America is 92 MtC·y−1. These estimates of gross emissions correspond well with the national estimates reported by Brazil, however, they are less than half of those reported in a recent study based on the FAO country statistics, highlighting the need for continued research in this area

Enzymfreisetzung und Aktivierung der Kallikrein-Kinin-Systeme bei experimenteller Pankreatitis

Das klinische Bild der akuten Pankreatitis wird entscheidend durch die sekundäre Schädigung von Herz-Kreislauf-System, Lunge und Niere bestimmt. Ziel der vorliegenden Untersuchung war es, durch Messungen in venösem Pankreasblut, Pankreaslymphe und Peritonealexsudat die Kompartimente zu bestimmen, über die die systemischen Schädigungen vermittelt werden. An anästhesierten Schweinen wurden die systemischen, hämodynamischen Parameter durch gesteuerte Volumentherapie konstant gehalten. Die Schweine wurden randomisiert der Kontrollgruppe (n = 9) oder einer der Pankreatitisgruppen zugeteilt (jeweils n = 10). Die Pankreatitis wurde durch Infusion von freier Fettsäure in die Pankreasarterien (FFS) oder durch Infusion einer 5%igen Natrium-Taurocholat-Lösung retrograd in den Pankreasgang (NaT) ausgelöst. Nach Isolation des Pankreas wurde venöses Pankreasblut, Pankreaslymphe und Peritonealexsudat gewonnen und die Aktivität von Lipase, Phospholipase A und Plasmaprokallikrein sowie die Konzentration von Organkallikrein und Kininogen bestimmt. In beiden Pankreatitismodellen fand sich ein Anstieg der Enzymaktivitäten. Die höchsten Aktivitäten fanden sich im Peritonealexsudat (Phospholipase A nach 40 min: Kontrolle 10,0 U/1, NaT 72,2 U/1). In beiden Pankreatitismodellen fanden sich außerdem Hinweise für eine Aktivierung des Organkallikrein-Kinin-Systems durch den Anstieg der Organkallikreinkonzentration und den Abfall der Gesamtkininogenkonzentration. Die stärksten Veränderungen fanden sich wieder im Peritonealexsudat (Organkallikrein nach 40 min: Kontrolle 14,7 ng/ml, NaT 452 ng/ml).The clinical course of acute pancreatitis is strongly influenced by secondary cardiac, pulmonary and renal damage. The aim of the present study was to gather information about the compartment promoting the systemic damage. Therefore the activity of lipase, phospholipase A and plasmaprokallikrein and the concentration of tissue kallikrein and kininogen were measured in portal venous blood, pancreatic lymph and peritoneal exudate. Anaesthetized pigs were subjected to fluid resuscitation to keep systemic haemodynamic parameters constant. The pancreas was isolated in situ. The pigs were randomly assigned to a control group (n = 9) or one of the two pancreatitis groups (n = 10 each). Pancreatitis was induced by i.a. infusion of free fatty acid (FFS) or retrograde infusion of 5 % sodium taurocholate intraductally (NaT). In both pancreatitis groups the activity of lipase and phospholipase A increased. The most pronounced changes were seen in the peritoneal exsudate (phospholipase A activity 40 min after induction: control 10.0 U/1, NaT 72.2 U/1). In both pancreatitis groups there was evidence for activation of the tissue kallikreinkinin system in the form of an increase in the kallikrein concentration and a decrease in the kininogen concentration. Again the changes were most pronounced in the peritoneal exsudate (tissue kallikrein 40 min after induction: control 14.7 ng/ml, NaT 452 ng/ml)

Velocity and density profiles of granular flow in channels using lattice gas automaton

We have performed two-dimensional lattice-gas-automaton simulations of granular flow between two parallel planes. We find that the velocity profiles have non-parabolic distributions while simultaneously the density profiles are non-uniform. Under non-slip boundary conditions, deviation of velocity profiles from the parabolic form of newtonian fluids is found to be characterized solely by ratio of maximal velocity at the center to the average velocity, though the ratio depends on the model parameters in a complex manner. We also find that the maximal velocity ($u_{max}$) at the center is a linear function of the driving force (g) as $u_{max} = \alpha g - \delta$ with non-zero $\delta$ in contrast with newtonian fluids. Regarding density profiles, we observe that densities near the boundaries are higher than those in the center. The width of higher densities (above the average density) relative to the channel width is a decreasing function of a variable which scales with the driving force (g), energy dissipation parameter ($\epsilon$) and the width of the system (L) as $g^{\mu} L^{\nu}/\epsilon$ with exponents $\mu = 1.4 \pm 0.1$ and $\nu = 0.5 \pm 0.1$. A phenomenological theory based on a scaling argument is presented to interpret these findings.Comment: Latex, 15 figures, to appear in PR

The effect of influenza and pneumococcal vaccination in the elderly on health service utilisation and costs: a claims data-based cohort study

Background: To date, cost-effectiveness of influenza and pneumococcal vaccinations was assumed in several health economic modelling studies, but confirmation by real-world data is sparse. The aim of this study is to assess the effects on health care utilisation and costs in the elderly using real-world data on both, outpatient and inpatient care. Methods: Retrospective community-based cohort study with 138,877 individuals aged ≥ 60 years, insured in a large health insurance fund in Thuringia (Germany). We assessed health care utilisation and costs due to influenza- or pneumococcal-associated diseases, respiratory infections, and sepsis in 2015 and 2016. Individuals were classified into four groups according to their vaccination status from 2008 to 2016 (none, both, or either only influenza or pneumococcal vaccination). Inverse probability weighting based on 236 pre-treatment covariates was used to adjust for potential indication and healthy vaccinee bias. Results: Influenza vaccination appeared as cost-saving in 2016, with lower disease-related health care costs of − €178.87 [95% CI − €240.03;− €117.17] per individual (2015: − €50.02 [95% CI − €115.48;€15.44]). Cost-savings mainly resulted from hospital inpatient care, whereas higher costs occurred for outpatient care. Overall cost savings of pneumococcal vaccination were not statistically significant in both years, but disease-related outpatient care costs were lower in pneumococci-vaccinated individuals in 2015 [− €9.43; 95% CI − €17.56;− €1.30] and 2016 [− €12.93; 95% CI − €25.37;− €0.48]. Although we used complex adjustment, residual bias cannot be completely ruled out. Conclusion: Influenza and pneumococcal vaccination in the elderly can be cost-saving in selective seasons and health care divisions. As cost effects vary, interpretation of findings is partly challenging.Peer Reviewe